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[PMID]:29330562
[Au] Autor:Zhao L; Zhu H; Han B; Wang L; Sun Y; Lu X; Huang C; Tan B; Chen C; Qin L
[Ad] Endereço:Department of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, 610041, People's Republic of China.
[Ti] Título:Influence of genetic polymorphisms of IL23R, STAT3, IL12B, and STAT4 on the risk of aplastic anemia and the effect of immunosuppressive therapy.
[So] Source:Ann Hematol;97(4):685-695, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Studies have suggested that IL-23/STAT3 and IL-12/STAT4 signaling pathways associate with aplastic anemia (AA) occurrence. Polymorphisms in pathway-related genes may contribute to AA risk. In the current study, we investigated the association between polymorphisms in genes of IL23R, STAT3, IL12B, and STAT4 and occurrence, severity, and immunosuppressive outcome of AA in the Han population in southwest China. In the current 164 AA cases and 211 controls study, we found T allele and TT genotype of rs7574865 were more frequent in the cases than that in the controls. In the additive model, individual carrying rs7574865 T allele demonstrated a 37% (OR (95% CI) = 1.37 (1.02-1.85), Pper = 0.036) increased AA risk. In the recessive model, carrier with rs7574865 TT genotype showed a 2.08-fold increased AA risk (OR (95% CI) = 2.08 (1.14-3.70), Pper = 0.017). Additionally, we showed that G allele and GG genotype of rs11209032 were more frequent in the 88 non-severe AA cases than that in the 76 severe AA ones. Our study also found G allele and GG genotype of rs11209032, and GG-genotype of rs744166 associated with the immunosuppressive therapy outcome in AA patients. Current study results support that functional STAT4 (rs7574865), IL23R (rs11209032), and STAT3 (rs744166) variants may associate with occurrence, severity, and immunosuppressive outcome of AA in the Han population in southwest China.
[Mh] Termos MeSH primário: Anemia Aplástica/genética
Anemia Aplástica/terapia
Imunossupressão
Polimorfismo de Nucleotídeo Único
Receptores de Interleucina/genética
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT4/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Anemia Aplástica/imunologia
Anemia Aplástica/fisiopatologia
Grupo com Ancestrais do Continente Asiático
Estudos de Casos e Controles
China
Feminino
Seguimentos
Estudos de Associação Genética
Predisposição Genética para Doença
Seres Humanos
Subunidade p40 da Interleucina-12/genética
Masculino
Meia-Idade
Estudos Retrospectivos
Índice de Gravidade de Doença
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (IL12B protein, human); 0 (IL23R protein, human); 0 (Interleukin-12 Subunit p40); 0 (Receptors, Interleukin); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (STAT4 Transcription Factor); 0 (STAT4 protein, human)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180114
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-018-3227-7


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[PMID]:29248579
[Au] Autor:Girardelli M; Basaldella F; Paolera SD; Vuch J; Tommasini A; Martelossi S; Crovella S; Bianco AM
[Ad] Endereço:Institute for Maternal and Child Health - IRCCS "Burlo Garofolo", Via dell'istria 65, Trieste, Italy.
[Ti] Título:Genetic profile of patients with early onset inflammatory bowel disease.
[So] Source:Gene;645:18-29, 2018 Mar 01.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Inflammatory Bowel disease (IBD) is a widespread pathological condition with clinical heterogeneity and with different levels of severity. Although IBD usually occurs in young adults, onset in childhood and infancy are described in patients within the 10th and second year of age. By genome-wide association studies and meta-analysis, several genetic loci have been identified associated with an increased risk of developing IBD in Western populations with variants that may alter the normal mucosal immunity in the gastrointestinal tract. The clinical complexity and the heterogeneity of the IBD phenotype probably reflect the presence of genetic heterogeneity where different genes or combinations of them may be involved, together with environmental factors. We hypothesized that patients with early onset IBD could have either more severe genetic variants in genes associated with IBD or multiple variants in different genes. Under the multifactorial diseases is crucial to consider the small contribution of a single variant in all not only to other small variations in the same gene but also in different genes belonging to the same pathway. We performed direct gene sequencing looking for 94 variations in NOD2, ATG16L1, IL23R, IL10R, IL10 and XIAP genes previously shown as correlated with IBD both in multifactorial and in Mendelian models. All variants identified are known in literature as being associated with IBD except for three variants in the genes NOD2, IL10 and IL10RB that even though present in online databases have never been involved in association studies on IBD patients. Moreover, we coupled genetic variants identification with an accurate "in silico" analysis to verify their predictive impact on the protein structure and function. The in-silico prediction of these variants results as benign therefore even if they exhibit a very low frequency in control population being benign, they cannot be considered pathogenic as monogenic disease but fall within the multifactorial range. The variants identified in our study partially reflect the association data described in the literature but there are no significant differences with the onset of disease (VEO vs EO-IBD).
[Mh] Termos MeSH primário: Predisposição Genética para Doença/genética
Doenças Inflamatórias Intestinais/genética
Polimorfismo de Nucleotídeo Único
Análise de Sequência de DNA/métodos
[Mh] Termos MeSH secundário: Idade de Início
Proteínas Relacionadas à Autofagia/genética
Criança
Pré-Escolar
Simulação por Computador
Feminino
Estudo de Associação Genômica Ampla
Seres Humanos
Lactente
Interleucina-10/genética
Masculino
Proteína Adaptadora de Sinalização NOD2/genética
Receptores de Interleucina/genética
Receptores de Interleucina-10/genética
Proteínas Inibidoras de Apoptose Ligadas ao Cromossomo X/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATG16L1 protein, human); 0 (Autophagy-Related Proteins); 0 (IL10 protein, human); 0 (IL23R protein, human); 0 (NOD2 protein, human); 0 (Nod2 Signaling Adaptor Protein); 0 (Receptors, Interleukin); 0 (Receptors, Interleukin-10); 0 (X-Linked Inhibitor of Apoptosis Protein); 0 (XIAP protein, human); 130068-27-8 (Interleukin-10)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171218
[St] Status:MEDLINE


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[PMID]:29187586
[Au] Autor:Banerjee A; Bhattacharya P; Dagur PK; Karmakar S; Ismail N; Joshi AB; Akue AD; KuKuruga M; McCoy JP; Dey R; Nakhasi HL
[Ad] Endereço:Division of Emerging and Transfusion Transmitted Diseases, Office of Blood Research and Review, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, MD 20993.
[Ti] Título:Live Attenuated Centrin Gene-Deleted Parasites Induce IL-23-Dependent IL-17-Protective Immune Response against Visceral Leishmaniasis in a Murine Model.
[So] Source:J Immunol;200(1):163-176, 2018 01 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:No vaccine exists against visceral leishmaniasis. To develop effective vaccines, we have previously reported protective role of live attenuated centrin gene-deleted ( ) parasites through induction of Th1 type immune response in mice, hamsters, and dogs. In this study, we specifically explored the role of Th17 cells in -induced host protection in mice. Our results showed that compared with wild-type infection, parasites induce significantly higher expression of Th17 differentiation cytokines in splenic dendritic cells. There was also induction of IL-17 and its promoting cytokines in total splenocytes and in both CD4 and CD8 T cells following immunization with Upon challenge with wild-type parasites, IL-17 and its differentiating cytokines were significantly higher in -immunized mice compared with nonimmunized mice that resulted in parasite control. Alongside IL-17 induction, we observed induction of IFN-γ-producing Th1 cells as reported earlier. However, Th17 cells are generated before Th1 cells. Neutralization of either IL-17 or IFN-γ abrogated -induced host protection further confirming the essential role of Th17 along with Th1 cytokines in host protection. Treatment with recombinant IL-23, which is required for stabilization and maintenance of IL-17, heightened Th17, and Tc17 responses in immunized mice splenocytes. In contrast, Th17 response was absent in immunized IL-23R mice that failed to induce protection upon virulent challenge suggesting that IL-23 plays an essential role in IL-17-mediated protection by parasites. This study unveiled the role of IL-23-dependent IL-17 induction in parasite-induced immunity and subsequent protection against visceral leishmaniasis.
[Mh] Termos MeSH primário: Interleucina-17/metabolismo
Interleucina-23/metabolismo
Leishmania donovani/imunologia
Vacinas contra Leishmaniose/imunologia
Leishmaniose Visceral/imunologia
Células Th1/imunologia
Células Th17/imunologia
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Feminino
Seres Humanos
Leishmania donovani/genética
Vacinas contra Leishmaniose/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteínas de Protozoários/genética
Receptores de Interleucina/genética
Células Th1/parasitologia
Células Th17/parasitologia
Vacinas Atenuadas/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Interleukin-17); 0 (Interleukin-23); 0 (Leishmaniasis Vaccines); 0 (Protozoan Proteins); 0 (Receptors, Interleukin); 0 (Vaccines, Attenuated); 0 (interleukin-23 receptor, mouse)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700674


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[PMID]:29045903
[Au] Autor:Osbourn M; Soares DC; Vacca F; Cohen ES; Scott IC; Gregory WF; Smyth DJ; Toivakka M; Kemter AM; le Bihan T; Wear M; Hoving D; Filbey KJ; Hewitson JP; Henderson H; Gonzàlez-Cìscar A; Errington C; Vermeren S; Astier AL; Wallace WA; Schwarze J; Ivens AC; Maizels RM; McSorley HJ
[Ad] Endereço:MRC Centre for Inflammation Research, University of Edinburgh, Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK.
[Ti] Título:HpARI Protein Secreted by a Helminth Parasite Suppresses Interleukin-33.
[So] Source:Immunity;47(4):739-751.e5, 2017 Oct 17.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Infection by helminth parasites is associated with amelioration of allergic reactivity, but mechanistic insights into this association are lacking. Products secreted by the mouse parasite Heligmosomoides polygyrus suppress type 2 (allergic) immune responses through interference in the interleukin-33 (IL-33) pathway. Here, we identified H. polygyrus Alarmin Release Inhibitor (HpARI), an IL-33-suppressive 26-kDa protein, containing three predicted complement control protein (CCP) modules. In vivo, recombinant HpARI abrogated IL-33, group 2 innate lymphoid cell (ILC2) and eosinophilic responses to Alternaria allergen administration, and diminished eosinophilic responses to Nippostrongylus brasiliensis, increasing parasite burden. HpARI bound directly to both mouse and human IL-33 (in the cytokine's activated state) and also to nuclear DNA via its N-terminal CCP module pair (CCP1/2), tethering active IL-33 within necrotic cells, preventing its release, and forestalling initiation of type 2 allergic responses. Thus, HpARI employs a novel molecular strategy to suppress type 2 immunity in both infection and allergy.
[Mh] Termos MeSH primário: Proteínas de Helminto/imunologia
Interleucina-33/imunologia
Nematospiroides dubius/imunologia
Infecções por Strongylida/imunologia
[Mh] Termos MeSH secundário: Alérgenos/imunologia
Alternaria/imunologia
Sequência de Aminoácidos
Animais
Western Blotting
Eosinófilos/imunologia
Proteínas de Helminto/genética
Proteínas de Helminto/metabolismo
Interações Hospedeiro-Parasita/imunologia
Seres Humanos
Imunidade Inata/imunologia
Interleucina-33/genética
Interleucina-33/metabolismo
Linfócitos/imunologia
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Knockout
Nematospiroides dubius/genética
Nematospiroides dubius/metabolismo
Ligação Proteica/imunologia
Receptores de Interleucina/imunologia
Receptores de Interleucina/metabolismo
Homologia de Sequência de Aminoácidos
Infecções por Strongylida/metabolismo
Infecções por Strongylida/parasitologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Allergens); 0 (Helminth Proteins); 0 (Interleukin-33); 0 (Receptors, Interleukin); 0 (interleukin-33 receptor, mouse)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171019
[St] Status:MEDLINE


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[PMID]:28877988
[Au] Autor:Geha M; Tsokos MG; Bosse RE; Sannikova T; Iwakura Y; Dalle Lucca JJ; De Waal Malefyt R; Tsokos GC
[Ad] Endereço:Department of Pediatrics, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114.
[Ti] Título:IL-17A Produced by Innate Lymphoid Cells Is Essential for Intestinal Ischemia-Reperfusion Injury.
[So] Source:J Immunol;199(8):2921-2929, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ischemia-reperfusion (IR) injury to the small intestine following clamping of the superior mesenteric artery results in an intense local inflammatory response that is characterized by villous damage and neutrophil infiltration. IL-17A, a cytokine produced by a variety of cells in response to inflammatory cytokines released following tissue injury, has been implicated in IR injury. Using , , and mice and administration of anti-IL-17A and anti-IL-23 neutralizing Abs to wild-type mice, we demonstrate that intestinal IR injury depends on IL-17A and that IL-17A is downstream of the binding of autoantibody to ischemia-conditioned tissues and subsequent complement activation. Using bone marrow chimeras, we demonstrate that the IL-17A required for intestinal IR injury is derived from hematopoietic cells. Finally, by transferring autoantibody-rich sera into and mice, we demonstrate that innate lymphoid cells are the main producers of IL-17A in intestinal IR injury. We propose that local production of IL-17A by innate lymphoid cells is crucial for the development of intestinal IR injury and may provide a therapeutic target for clinical exploitation.
[Mh] Termos MeSH primário: Interleucina-17/metabolismo
Intestino Delgado/imunologia
Intestino Delgado/patologia
Linfócitos/imunologia
Traumatismo por Reperfusão/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Bloqueadores/administração & dosagem
Autoanticorpos/metabolismo
Células Cultivadas
Ativação do Complemento
Proteínas de Ligação a DNA/genética
Modelos Animais de Doenças
Seres Humanos
Imunidade Inata
Interleucina-17/genética
Artéria Mesentérica Superior/cirurgia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Infiltração de Neutrófilos
Membro 3 do Grupo F da Subfamília 1 de Receptores Nucleares/genética
Receptores de Interleucina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Blocking); 0 (Autoantibodies); 0 (DNA-Binding Proteins); 0 (Interleukin-17); 0 (Nuclear Receptor Subfamily 1, Group F, Member 3); 0 (Rag2 protein, mouse); 0 (Receptors, Interleukin); 0 (Rorc protein, mouse); 0 (interleukin-23 receptor, mouse)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700655


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[PMID]:28855314
[Au] Autor:Muschaweckh A; Petermann F; Korn T
[Ad] Endereço:Klinikum Rechts der Isar, Neurologische Klinik, Technische Universität München, 81675 Munich, Germany; and.
[Ti] Título:IL-1ß and IL-23 Promote Extrathymic Commitment of CD27 CD122 γδ T Cells to γδT17 Cells.
[So] Source:J Immunol;199(8):2668-2679, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:γδT17 cells are a subset of γδ T cells committed to IL-17 production and are characterized by the expression of IL-23R and CCR6 and lack of CD27 expression. γδT17 cells are believed to arise within a narrow time window during prenatal thymic development. In agreement with this concept, we show in this study that adult recipient mice of (IL-23R reporter) bone marrow selectively lack IL-23R γδT17 cells. Despite their absence in secondary lymphoid tissues during homeostasis, γδT17 cells emerge in bone marrow chimeric mice upon induction of skin inflammation by topical treatment with imiquimod cream (Aldara). We demonstrate that IL-1ß and IL-23 together are able to promote the development of bona fide γδT17 cells from peripheral CD122 IL-23R γδ T cells, whereas CD122 γδ T cells fail to convert into γδT17 cells and remain stable IFN-γ producers (γδT1 cells). IL-23 is instrumental in expanding extrathymically generated γδT17 cells. In particular, TCR-Vγ4 chain-expressing CD122 IL-23R γδ T cells are induced to express IL-23R and IL-17 outside the thymus during skin inflammation. In contrast, TCR-Vγ1 γδ T cells largely resist this process because prior TCR engagement in the thymus has initiated their commitment to the γδT1 lineage. In summary, our data reveal that the peripheral pool of γδ T cells retains a considerable degree of plasticity because it harbors "naive" precursors, which can be induced to produce IL-17 and replenish peripheral niches that are usually occupied by thymus-derived γδT17 cells.
[Mh] Termos MeSH primário: Interleucina-17/metabolismo
Psoríase/imunologia
Linfócitos T/fisiologia
[Mh] Termos MeSH secundário: Aminoquinolinas
Animais
Diferenciação Celular
Células Cultivadas
Modelos Animais de Doenças
Seres Humanos
Interleucina-1beta/metabolismo
Subunidade beta de Receptor de Interleucina-2/metabolismo
Interleucina-23/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores de Antígenos de Linfócitos T gama-delta/metabolismo
Receptores de Interleucina/genética
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminoquinolines); 0 (Interleukin-17); 0 (Interleukin-1beta); 0 (Interleukin-2 Receptor beta Subunit); 0 (Interleukin-23); 0 (Receptors, Antigen, T-Cell, gamma-delta); 0 (Receptors, Interleukin); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 0 (interleukin-23 receptor, mouse); P1QW714R7M (imiquimod)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700287


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[PMID]:28832218
[Au] Autor:Al Efraij K; FitzGerald JM
[Ad] Endereço:a Faculty of Medicine, Division of Respirology , University of British Columbia , Vancouver , BC , Canada.
[Ti] Título:Emerging interleukin receptor antagonists for the treatment of asthma.
[So] Source:Expert Opin Emerg Drugs;22(3):275-283, 2017 Sep.
[Is] ISSN:1744-7623
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Asthma is a heterogeneous disease, usually characterized by chronic airway inflammation. Most patients with asthma can be well-controlled with inhaled corticosteroids and, if necessary, the addition of a long-acting beta agonist. Despite these therapies, 5% to 10% of patients with asthma have severe, uncontrolled asthma. Selecting patients based on peripheral eosinophil counts and a history of exacerbations has led to significant decreases in exacerbations and an improvement in asthma control with medications that target IL-4, IL-5 and IL-13/. Areas covered: This review will cover the definition of severe asthma, existing treatment options, biomarkers, and the emerging role of interleukin antagonists in the treatment of severe asthma. Expert opinion: IL antagonists are novel drugs targeting important inflammatory cytokines in asthma. Anti-IL-5 drugs provide the most promise as they have obtained regulatory approval and are available for use. Anti-IL-4 drug results are also promising. There is, however, uncertainty regarding the success of anti-IL-13 drugs development at this point. An ongoing focus of research is to significantly increase our understanding of the biology of asthma, and in particular severe asthma, making more and better targeted therapies. There may also be potential in the future to use these new drugs earlier in the development of asthma, as disease-modifying interventions that might be associated with remission or even cure.
[Mh] Termos MeSH primário: Antiasmáticos/uso terapêutico
Asma/tratamento farmacológico
Receptores de Interleucina/antagonistas & inibidores
[Mh] Termos MeSH secundário: Antiasmáticos/farmacologia
Asma/fisiopatologia
Biomarcadores/metabolismo
Citocinas/metabolismo
Seres Humanos
Interleucina-13/imunologia
Interleucina-4/imunologia
Interleucina-5/imunologia
Receptores de Interleucina/imunologia
Índice de Gravidade de Doença
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Asthmatic Agents); 0 (Biomarkers); 0 (Cytokines); 0 (Interleukin-13); 0 (Interleukin-5); 0 (Receptors, Interleukin); 207137-56-2 (Interleukin-4)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1080/14728214.2017.1369954


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[PMID]:28771607
[Au] Autor:Park SK; Jin YD; Park YK; Yeon SH; Xu J; Han RN; Rha KS; Kim YM
[Ad] Endereço:Department of Otorhinolaryngology-Head and Neck Surgery, Research Institute for Medical Science, Chungnam National University School of Medicine, Daejeon, Korea.
[Ti] Título:IL-25-induced activation of nasal fibroblast and its association with the remodeling of chronic rhinosinusitis with nasal polyposis.
[So] Source:PLoS One;12(8):e0181806, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND OBJECTIVE: Interleukin (IL)-25 has been shown to play an important role in the pathogenesis of chronic rhinosinusitis with nasal polyps. Nasal polyps are associated with chronic inflammation of the mucous membranes in the paranasal sinuses and are involved in extracellular matrix (ECM) accumulation. The aim of this study is to evaluate the effects of IL-25 on myofibroblast differentiation, ECM production and the expression of matrix metalloproteinases in nasal polyp derived fibroblasts (NPDFs) and to determine the molecular mechanism underlying these processes. MATERIALS AND METHODS: A total of 40 patients were enrolled in this study for Immunofluorescence studies. Expression of IL17 receptor B was evaluated by real time reverse transcription polymerase chain reaction (PCR) in NPDFs. NPDFs were stimulated with IL-25 for 48 h in the presence or absence of mitogen-activated protein kinase (MAPK) and NF-κB inhibitors or small interfering RNAs (siRNA). The protein levels of fibrosis active mediators were examined using western blotting. Fibroblast migration was evaluated with a scratch assay. The total collagen amount was analyzed with the Sircol collagen assay. RESULTS: IL-25 induced α-SMA, fibronectin, and MMP-1 and -13, which were dependent on IL-17RB. IL-25 also induced activation of NF-κB and mitogen-activated protein kinase (MAPKs). By using the specific inhibitor of ERK, p38, JNK and NF-κB (U, SB, SP and Bay), we found that IL-25-induced expressions of α-SMA, fibronectin, and MMPs was regulated by the signaling pathways of MAPKs and NF-κB. IL-25 also induces α-SMA, fibronectin, and MMPs expression through IL-17RB-dependent pathways in NPDFs. The increased migration ability induced by IL-25 was suppressed by the specific inhibitors of MAPKs and NF-κB. CONCLUSION: Our data indicate that IL-25 induced myofibroblast differentiation, fibronectin production, and MMP-1 and -13 expressions through the signaling pathways of MAPKs and NF-κB. in NPDFs and increased expression of IL-25 were also involved in the pathogenesis of nasal polyposis by affecting nasal fibroblasts in chronic rhinosinusitis with nasal polyps.
[Mh] Termos MeSH primário: Fibroblastos/efeitos dos fármacos
Fibroblastos/patologia
Interleucina-17/farmacologia
Pólipos Nasais/complicações
Nariz/patologia
Sinusite/patologia
[Mh] Termos MeSH secundário: Actinas/metabolismo
Adulto
Diferenciação Celular/efeitos dos fármacos
Movimento Celular/efeitos dos fármacos
Ativação Enzimática/efeitos dos fármacos
Feminino
Fibronectinas/biossíntese
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Masculino
Metaloproteinase 1 da Matriz/metabolismo
Metaloproteinase 13 da Matriz/metabolismo
Meia-Idade
Proteínas Quinases Ativadas por Mitógeno/metabolismo
NF-kappa B/metabolismo
Receptores de Interleucina/genética
Receptores de Interleucina-17/metabolismo
Transdução de Sinais/efeitos dos fármacos
Sinusite/genética
Sinusite/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Fibronectins); 0 (IL-25 receptor protein, human); 0 (Interleukin-17); 0 (NF-kappa B); 0 (Receptors, Interleukin); 0 (Receptors, Interleukin-17); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.24.- (Matrix Metalloproteinase 13); EC 3.4.24.7 (Matrix Metalloproteinase 1)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181806


  9 / 4393 MEDLINE  
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[PMID]:28754339
[Au] Autor:Kulkarni NN; Adase CA; Zhang LJ; Borkowski AW; Li F; Sanford JA; Coleman DJ; Aguilera C; Indra AK; Gallo RL
[Ad] Endereço:Department of Dermatology, University of California, San Diego, California, USA.
[Ti] Título:IL-1 Receptor-Knockout Mice Develop Epidermal Cysts and Show an Altered Innate Immune Response after Exposure to UVB Radiation.
[So] Source:J Invest Dermatol;137(11):2417-2426, 2017 Nov.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study, we observed that mice lacking the IL-1 receptor (IL-1R) (IL1r ) or deficient in IL1-ß developed multiple epidermal cysts after chronic UVB exposure. Cysts that developed in IL1r mice were characterized by the presence of the hair follicle marker Sox 9, keratins 10 and 14, and normal melanocyte distribution and retinoid X receptor-α expression. The increased incidence of cysts in IL1r mice was associated with less skin inflammation as characterized by decreased recruitment of macrophages, and their skin also maintained epidermal barrier function compared with wild-type mice. Transcriptional analysis of the skin of IL1r mice after UVB exposure showed decreased gene expression of proinflammatory cytokines such as tumor necrosis factor-α and IL-6. In vitro, primary keratinocytes derived from IL1r mice were more resistant to UVB-triggered cell death compared with wild-type cells, and tumor necrosis factor-α release was completely blocked in the absence of IL-1R. These observations illustrate an unexpected yet prominent phenotype associated with the lack of IL-1R signaling in mice and support further investigation into the role of IL-1 ligands in epidermal repair and innate immune response after damaging UVB exposure.
[Mh] Termos MeSH primário: Cisto Epidérmico/radioterapia
Regulação da Expressão Gênica
Imunidade Inata/genética
Queratinócitos/imunologia
Queratinócitos/efeitos da radiação
Raios Ultravioleta/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Biópsia por Agulha
Western Blotting
Células Cultivadas
Dano ao DNA/efeitos da radiação
Modelos Animais de Doenças
Cisto Epidérmico/imunologia
Cisto Epidérmico/patologia
Feminino
Imuno-Histoquímica
Queratinócitos/patologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Distribuição Aleatória
Reação em Cadeia da Polimerase em Tempo Real
Receptores de Interleucina/deficiência
Receptores de Interleucina/imunologia
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Interleukin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170730
[St] Status:MEDLINE


  10 / 4393 MEDLINE  
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[PMID]:28715683
[Au] Autor:Ren L; Xu Y; Liu C; Wang S; Qin G
[Ad] Endereço:Department of Endocrinology, The First Affiliated Hospital of ZhengZhou University, Zhengzhou 450002, China.
[Ti] Título:IL-17RB enhances thyroid cancer cell invasion and metastasis via ERK1/2 pathway-mediated MMP-9 expression.
[So] Source:Mol Immunol;90:126-135, 2017 Oct.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:IL-17RB, a member of the IL-17 receptor family that can be activated by IL-17B, has been proved to be involved in inflammatory diseases and cancers. However, the function of IL-17RB in thyroid cancer is still unknown. In this study, IL-17RB expression in thyroid cancer cell lines and tissues was examined by real-time PCR and western blot. The effects of IL-17RB on cell invasion and migration were determined by in vitro invasion and migration assays, while the effects of IL-17RB on cell metastasis were analyzed by in vivo experiments. The results showed that IL-17RB expression was upregulated in both thyroid cancer cells and tissues. IL-17B dose-dependently promoted the invasion, growth and migration of thyroid cancer cells, whereas knockdown of IL-17RB attenuated the effects of IL-17B in vitro. Moreover, IL-17RB was involved in the metastasis and growth of thyroid cancer cells in vivo. In addition, IL-17RB induced ERK1/2 activation and increased MMP-9 expression in vitro and in vivo. Inhibition of ERK1/2 pathway blocked the IL-17RB-mediated thyroid cancer cell invasion and MMP-9 expression. Together, our findings demonstrate that IL-17RB can enhance thyroid cancer cell invasion and metastasis via ERK1/2 pathway-mediated MMP-9 expression, suggesting that IL-17RB may act as a potential therapeutic target for thyroid cancer therapy.
[Mh] Termos MeSH primário: Movimento Celular/genética
Regulação Neoplásica da Expressão Gênica/genética
Sistema de Sinalização das MAP Quinases/fisiologia
Metaloproteinase 9 da Matriz/biossíntese
Receptores de Interleucina/biossíntese
Neoplasias da Glândula Tireoide/patologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Seres Humanos
Interleucina-17/farmacologia
Camundongos
Camundongos SCID
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
Interferência de RNA
RNA Interferente Pequeno/genética
Receptores de Interleucina/genética
Glândula Tireoide/citologia
Glândula Tireoide/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL17B protein, human); 0 (IL17RB protein, human); 0 (Interleukin-17); 0 (RNA, Small Interfering); 0 (Receptors, Interleukin); EC 3.4.24.35 (MMP9 protein, human); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE



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